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Rapid Review STEP 1 > Micro Pharm > Flashcards

Micro Pharm Flashcards

1
Q

Difference between peniciliin G and V.

A

G = IV and IM. V = oral. pharmacology micro

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1
Q

Penicillin(mechanism,use,toxicity)

A

Bind penicillin-binding proteins(transpeptidases), block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema;hypersensitivy reaction, hemolytic anema. pharmacology micro

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2
Q

Oxacillin,Naficillin,Dicloxacillin(mechanism,use,toxicity)

A

bind transpeptidases, penicillanse resistant due to bukly r-group blocking B-Lactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis. pharmacology micro

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3
Q

Ampicillin, amoxicillin(mecanism,use,toxicity)

A

bind transpeptidases, wide spectrum and more penicillinase sensitive. combo with claculanic acid to protect from B-lactams;kills enterococci(HELPSS)H.iB, E.coli,Listera,Proteus,Salmonella,Shigella,enterococci;hypersensitivity reaction,rash,pseudomemrane colitis. pharmacology micro

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4
Q

Which has better bioavailibility; amoxicllin or ampicillin?

A

amOxicllin has better Oral bioavilability. pharmacology micro

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5
Q

What does clavulanic acid do?

A

B-lactamse inhibitor pharmacology micro

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6
Q

Ticarcillin,piperacillin(mechanism,use,toxicity)

A

transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods, use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction. pharmacology micro

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7
Q

List the B-lactamse inhibitors

A

(CAST) Clavulanic Acid, Sulbactam,Tazobactem. pharmacology micro

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8
Q

Cephalosporin(mechanism,use,toxiciity)

A

inhibit cell wall synthesis but are less susceptible to B-lactamases, are bactericidal;use depends on generation, there are four;hypersensitivty reactions, vitamin K defiency, increased nephrotoxicity of aminoglycosides. pharmacology micro

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9
Q

give use of cefazolin, cephalexin.

A

1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections. pharmacology micro

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10
Q

give use of cefoxitin, cefaclor,cefuroxime`

A

2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia. pharmacology micro

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11
Q

give use of ceftriaxone, cefotaxime,ceftazidime

A

3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas. pharmacology micro

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12
Q

give use of cefepime.

A

increased activity against pseudomonas and G+ bugs. pharmacology micro

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13
Q

Aztreonam(mechanism,use,toxicty)

A

a monobactem resistant to B-lactamases, prevents binding to PBP3 and is synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset. pharmacology micro

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14
Q

what transpeptidase inhibitor can be used in penicillin allergy?

A

aztreonam. pharmacology micro

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15
Q

imipenem/cilastatin,meropenem,etrapenem,doripenem(mechanism,use,toxicity)

A

broad spectrum, B-lactamase resistent but imipenem needs cilastatin to inhibit renal dehydropeptidase. later carbepenems do not;G+ cocci,G- rods, anerobes. used only in life threating events;skin rash, CNS toxicity, seizures. pharmacology micro

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16
Q

Vancomycin(mechanism,use,toxicty)

A

inhibits cell wall binding peptidoglycan formation by binding D-ala percursors, is bacterialcidal; G+ only, especially for multidrug resistant onces;NOT - nephrotoxicity, ototoxicity, thrombophlebitis, red man syndrome. pharmacology micro

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17
Q

How is redman syndrome prevented in vancomycin use?

A

slow infusion and rate and antihistamines. pharmacology micro

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18
Q

How does vancomycin resistant occur?

A

amino acid change of D-ala D-ala to D-ala D-lac. pharmacology micro

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19
Q

List antibiotic protein synthesis inhibitors

A

AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = Chloramphenicol, Clindamycin, Erythromycin, Linezolid. pharmacology micro

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20
Q

Gentamicin, neomycin, amikacin,tobramycin,streptomycin(mechanism,use,toxicity)

A

aminoglycosides, bacterialcidal, block translocation but require oxygen for uptake;ineffective in anaerobes,use in gram - rod infections and before bowel surgery; nephrotoxicty, NMJ block, ototoxicity, teratogen. pharmacology micro

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21
Q

how does resistenace to aminoglycosides occur?

A

transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation. pharmacology micro

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22
Q

tetracycline, doxycycline, demecycline,minocycline(mechanism, use, toxicity)

A

bacteriostatic, prevents aminoacyl-tRNA binds;Borrela, M. Pneuomo, Rickettsia, Chlamysia; can’t take with milk, antacids, iron because ions bind it, GI distress, discoloration of teeth, inhibition of bone growth, contraindication in pregnancy. pharmacology micro

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23
Q

how does resistance to tetracyclines occur?

A

decrease uptake into cells or increased efflux by pumps. pharmacology micro

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24
Q

Azithromycin, clarithromycin, erythromycin(mechanism,use,toxicity)

A

bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia. pharmacology micro

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25
Q

how does resitance to macrolides occur?

A

methylation of 23s rRNA binding site. pharmacology micro

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26
Q

Chloramphenicol(mechanism,use,toxicity)

A

Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent aplastic anemia, gray baby syndrome. pharmacology micro

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27
Q

what causes grey baby syndrome?

A

use of chloramphenicol in premature infants, they lack UDO-glucuronyl-transferase. pharmacology micro

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28
Q

How does resistance to chloramphenicol occur?

A

plasmid-encoded acetyltransferase. pharmacology micro

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29
Q

clindamycin(mechanism,use,toxicity)

A

Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections and oral anerobes; C. Diff infection, fever, diarrhea. pharmacology micro

30
Q

Sulfamethoxazole(SMX), sulfisoxazole, sulfadiazine(mechanism, use, toxicity)

A

Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, kernicterus, displaces other drugs from albumin. pharmacology micro

31
Q

how does resistance to sulfonamides occur?

A

altered bacterial dihydropteroate or increased PABA synthesis. pharmacology micro

32
Q

Trimethoprim(mechanism,use,toxicity)

A

Bacteriostatic, inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; megaloblastic anemia, leukopenia, granulocytopenia. pharmacology micro

33
Q

ciprofloxacin, norfloxacin, levofloxacin, etc…(mechanism, use, toxicity)

A

bactericidal, inhibits DNA gyrase(topo II and IV);G- rods of urinary and GI tracts, Neisseria, some G+;( lones hurt the bones) tenonitis and tendon rupture, superinfections, don’t give to kids or pregnant women due to cartilage damage. pharmacology micro

34
Q

how does resistance to fluroquinolones occur?

A

mutation in DNA gyrase or efflux pumps. pharmacology micro

35
Q

What groups are susceptible to fluorquinolone tendon rupture?

A

older than 60 or taking prednisone pharmacology micro

36
Q

Metronidazole(mechanism, use, toxicity)

A

bacterialcidal, forms free radical toxic metabolites that damge bacterial DNA damage; (GET GAP) Giardia, Entamoeba, trichomonas, Gardnerella, Anaerobes, Pylori; causes disulfiram like reaction, headache, metallic taste. pharmacology micro

37
Q

Isoniazid(mechanism,use,toxicity)

A

decrease synthesis of mycolic acids, bacterial catalase peroxidase(KatG) must activate INH; TB drug, only one used as prophylaxis and in latent TB; peripheral neuropathy, hepatoxic, lupis like drug interaction, pyridoxine antagonist. pharmacology micro

38
Q

Rifampin(mechanism,use,toxicity)

A

inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids. pharmacology micro

39
Q

Pyrazinamide(mechanism, use, toxicity)

A

unknown; TB; hyperuricemia, hepatotoxic. pharmacology micro

40
Q

Ethambutol(mechanism,use,toxicity)

A

decreased carbohydrate polymerization of TB cell wall, blocks arabinosyltransferase; TB; optic neuropathy(red-green color blindness_ pharmacology micro

41
Q

Amphotericin B(mechanism, use, toxicity)

A

binds fungal ergosterol, causes holes in membranes; use in systemtic and CNS mycoses infections; fever/chills, hypotension, arrythmias, nephrotoxic, IV phlebitis, must supplement K and MG. pharmacology micro

42
Q

nystatin(mechanism,use,toxicty)

A

binds fungal ergosterol;topical only due to high toxicity, used for oral thrush and topical diaper rash or vaginal candidiasis. pharmacology micro

43
Q

Fluconazole, ketoconazole, clotrimazole, itraconazole, voriconazole(mechanism, use,toxicity)

A

inhibits fungal ergosterol synthesis by binding p450;Fluconazole for suppression of cryptococcus in AIDs patients, itraconazle for blasto, coccio, histo. pharmacology micro

44
Q

Flucytosine(mechanism, use, toxicity)

A

inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic fungal infections, especially cryptococcus; bone marrow suppression. pharmacology micro

45
Q

Caspofungin, micafungin(mechanism, use, toxicity)

A

inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive aspergillosis, candida; flushing via histamine releae. pharmacology micro

46
Q

terbinafine(mechanism,use,toxicity)

A

inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection especially;abnormal LFT, visual disturbances. pharmacology micro

47
Q

Griseofulvin(mechanism,use,toxicity)

A

interferes with microtubules, stops mitosis in fungi;deposits in keratin so used in superficial infections, stops dermatophytes; teratogenic, carcinogenic, confusion, p450 inducer. pharmacology micro

48
Q

Pyrimethamine use

A

toxoplasmosis pharmacology micro

49
Q

suramin and melarsoprol use

A

trypanosoma brucei pharmacology micro

50
Q

nifurtimox use

A

trypanosoma cruzi pharmacology micro

51
Q

sodium stibogluconate use

A

leshmaniasis pharmacology micro

52
Q

Chloroquine(mechanism,use,toxicity)

A

blocks formation of heme into hemozoin. Heme accumulates and is toxic to plasmodia;used on all species but falciparum(too much resitance); retinopathy pharmacology micro

53
Q

quinidine use

A

lifethreatening malaria pharmacology micro

54
Q

artemether/lumifantrine use

A

p. falciparum killing pharmacology micro

55
Q

Zanamivir,oseltamivir(mechanism,use)

A

inihibits influenza neuraminidase, stops progeny release; treamt of influenze a and b pharmacology micro

56
Q

Ribavarin(mechanism,use,toxicity)

A

inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen pharmacology micro

57
Q

Acyclovir,valacyclovir(mechanism, use, toxicity)

A

Guanosine analog, inhibits viral DNA polymerase; monophosphorylated by thymidine kinase in HSV/VZV so active in lesions and encephalitis, good for prophylaxis, pharmacology micro

58
Q

Famciclovir use

A

used in herpes zoster active infections pharmacology micro

59
Q

mechanism for resistance to acyclovir

A

mutated viral thymidine kinase pharmacology micro

60
Q

Ganciclovir,valgangciclovir(mechanism,use,toxicity)

A

guanosine analog, 5’-monophosphate formed by CMV viral kinase, inhibits viral DNA polymerase;CMV infections;leukopenia,neutopenia,thrombocytopenia,renal toxicity pharmacology micro

61
Q

mechanism for resistance to acyclovir

A

mutated CMV DNA polymerase or lack of viral kinase pharmacology micro

62
Q

Foscarnet(mechanism,use,toxicity)

A

viral DNA polymerase inhibitor, binds to pyrofosphate binding site, doesn’t need viral kinase activation;CMV retinitis when ganciclovir fails and acyclovir restitant HSV; nephrotoxic pharmacology micro

63
Q

mechanism for resistance to foscarnet

A

mutated DNA polymerase pharmacology micro

64
Q

cidofovir(mechanism,use,toxicity)

A

inhibits DNA polymerase, doesn’t require activiation by viral kinase; CMV retenitis, acyclovir resistant HSV; nephrotoxic pharmacology micro

65
Q

HAART consist of what?

A

[2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor] pharmacology micro

66
Q

give mechanism and toxicity of protease inhibitors

A

all end in -NAVIR! stops HIV mRNA cleavage into functional parts; hyperglycemia, GI upset, lipodystrophy. pharmacology micro

67
Q

Ritonavir does what to be a “booster”

A

inhibits cytochrome p-450, boosting concentration of other drugs. pharmacology micro

68
Q

Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didansoine, stavudine(mechanism,use,toxicity

A

(NRTI)competitively blocks binding of nucleotide to reverse transcriptase, only tenofovir doesn’t need to be activated;all NRTIs, zidovidine used in pregnancy to reduce fetal transmision; bone marrow suppression, lactic acidosis, peripheral neuropathy. pharmacology micro

69
Q

Nevirapine, Efavirenz, Delavirdine(mechanism,use,toxicity)

A

(NNRTI) bind at a site different from NRTIs, no don’t require activation don’t compete with nucleotides; bonow marrow suppression, peripheral neuropathy, lactic acidosis, pharmacology micro

70
Q

Raltegravir(mechanism,use,toxicity)

A

inhibits integrase, which stops HIV integration into host cells;HIV;hypercholesterolemia pharmacology micro

71
Q

Interferons(mechanism,use,toxicity)

A

glycoproteins synthesized my virus infected cells, block RNA and DNA virus replication; INFa- chronic hep b and c, Kaposi sarcoma, IFN-b -MS, INF-gamma -NADPH oxidase defiency; neutropenia, myopathy. pharmacology micro

72
Q

What antibiotics must be avoided in pregnancy?

A

SAFe Children Take Really Good Care. sulfonamides(kericterus), aminoglycosides(ototox), fluoroquinolones(cartilage damage), Clarithromycin(embryotoxic), Tetracycline(teeth,bone damage),Ribavarin(teratogenic),Griseofulvin(teratogenic),Chloramphenicol(grey baby) pharmacology micro

Rapid Review STEP 1 (13 decks)

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